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1995 Fiscal Year Final Research Report Summary

Role of Ras and Ras-relatd protein for carcinogenesis of endometrial

Research Project

Project/Area Number 05671379
Research Category

Grant-in-Aid for General Scientific Research (C)

Allocation TypeSingle-year Grants
Research Field Obstetrics and gynecology
Research InstitutionKyshu University

Principal Investigator

KATO Kiyoko  Medical Institute of Bioregulation Kyushu Univ. Lecturer, 生体防御医学研究所, 助手 (10253527)

Co-Investigator(Kenkyū-buntansha) WAKE Norio  Medical Institute of Bioregulation Kyushu Univ. Professor, 生体防御医学研究所, 教授 (50158606)
Project Period (FY) 1993 – 1995
KeywordsRas / Singnal transduction / EGF recepter / Endmetrial carcinoma
Research Abstract

Since the majority of endometrial carcinomas do not contain any detectable ras mutations, the precise contribution of aberrant Ras function, if any, to endometerial carcinoma development remains to be determineed. Since there is considerable evidence that Ras-transformation is associated with a decreased requirement growth factors, we compared the growth response of endometrial carcinoma cells harboring wild type (Ishikawa cells)or mutated (HHUA cells)K-ras to epidermal growth factor (EGF). First, we determined that both tumor cells expressed comparable levels of the EGF receptor. Next, we observed that EGF could stimulate the growth of Ishikawa, but not HHUA,cells. Furthermore, EGF caused an elevation of Ras-GTP levels in Ishikawa, but not HHUA,cells. However, the introduction of mutated, but not normal, K-ras into Ishikawa cells rendered them nonresponsive to EGF growth stimulation. Thus, the presence of mutated K-ras alone, can modulate the growth response of endometrial carcinoma cells to EGF.Finally, we observed that an inhibitor of the EGF receptor tyrosine kinase activity could prevent soft agar colony formation of Ishikawa cells, but not HHUA or mutant K-ras(12V)-transfected Ishikawa cells. Taken together, these results suggest that mutated K-ras causes a loss of responsiveness to EGF stimulation and that EGTF receptor function is now dispensable for the growth of mutant Ras-positive endometrial carcinoma cells.

  • Research Products

    (8 results)

All Other

All Publications (8 results)

  • [Publications] N. Wake: "Accumulation of Genetic Events in Endometrial Carcinoma andits Cell Growth Inhibition by Antisense Oligonucleotide Complementary to the Mutated K- ras Gene." Cancer Molecular Biology. 1. 145-156 (1994)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] T. Arima: "Genetic origin of malignant trophoblastic neoplasms." Cancer Genet cytogenet. 73. 5-12 (1994)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] T. Arima: "Malignant trophoblastic neoplasms with different modes of origin." Cancer Genet Cytogenet. 85. 5-15 (1995)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] T. Arima: "Association of IGF2 and H19 imprinting with choriocarcinoma development." Human Genet. (Submitted).

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] N.Wake: "Accumlation of Genetic Events in Endometrial Carcinoma andits Cell Growth Inhibition by Antisense Oligonucleotide Complementary to theMutated K-ras Gene" Cancer Molecular Biology. 1. 145-156 (1994)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] T.Arima: "Genetic origin of malignant trophoblastic neoplasms." Cancer Genet Cytogenet. 73. 5-12 (1994)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] Arima, T: "Malignant trophoblkastic neoplasms with different modes of origin." Cancer Genet Cytogenet. 85. 5-15 (1995)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] Arima, T: "Association of IGF2 and H19 imprinting with choriocarcinoma development." Human Genet. (Submitted).

    • Description
      「研究成果報告書概要(欧文)」より

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Published: 1997-03-04  

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